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PubMed1997

Gamma activity in the piriform cortex and behavioral thresholds for electrical stimulation in the olfactory bulb.

The olfactory bulb was stimulated by trains of electrical pulses in freely moving rats. Evoked responses resembling damped oscillations at the gamma frequency of 30-60 Hz were recorded in the anterior and posterior piriform cortex. Different types of unconditioned sniffing were induced by stimulation of the olfactory bulb. They were similar to those evoked by an odorant (amylacetate) but differed from the behavioral patterns evoked by non-olfactory (auditory) stimulation. Rats were trained to avoid foot-shocks following electrical pulses into the olfactory bulb as conditioned stimulus in a two way shuttle-box paradigm. Threshold electrical intensities for inducing evoked responses in piriform cortex, unconditioned behavior, and learned avoidance were compared. Thresholds for unconditioned and conditioned behavior were significantly higher in comparison with those for evoking gamma discharges in anterior and posterior piriform cortex. The results suggest that fast time-locked synchronization in the gamma range in the piriform cortex induced by synaptic input from theolfactory bulb is not sufficient for inducing corresponding behavior. Thus behavioral detection and probably also olfactory recognition do not seem to be direct consequences of this fast time-locked neural synchronization. Additional neuronal processes that are connected with further elevation of stimulation intensity seem to be necessary for that.

Animals↗
PubMed1999

The piriform cortex and the endopiriform nucleus in the rat reveal generally similar pattern of connections.

The afferent and efferent connections of the piriform cortex and the endopiriform nucleus in the rat were studied by the method of axonal transport of two fluorescent tracers: Fluoro-Gold and Fluoro-Ruby. The results indicate that both structures possess not only the connections with the olfactory system, but also the reciprocal connections with the limbic system (entorhinal cortex, amygdaloid body), thalamus (mediodorsal and midline nuclei), extrapyramidal system (ventral part of the nucleus accumbens). The topographic differences in the organization of the association connections between the anterior and posterior parts of the piriform cortex are reported. Additionally, the reciprocal and relatively numerous connections between the endopiriform nucleus and the piriform cortex may result in their modulatory function, which in some pathological circumstances may have a critical significance in epileptogenesis.

Afferent Pathways↗
PubMed1996

Kindling-induced epileptiform potentials in piriform cortex slices originate in the underlying endopiriform nucleus.

1. Previous studies in vivo and in vitro have shown that kindling from several locations in the limbic system induces the onset of epileptiform activity in the piriform (olfactory) cortex in the rat. In the present study we tested the hypothesis that kindled epileptiform events in piriform cortex are initiated in the underlying endopiriform nucleus. The experiments were performed in slices taken from rats that were previously kindled by conventional means. 2. Both stimulus-evoked and spontaneous interictal-like epileptiform events were observed in most slices from the anterior piriform cortex, but in few slices from the posterior piriform cortex. These events resembled those described in unanesthetized and urethan-anesthetized rats in previous studies. 3. Findings in support of the hypothesis were as follows. Epileptiform events in the endopiriform nucleus preceded those in the piriform cortex. Epileptiform events could occur in endopiriform nucleus alone, but were only observed in the piriform cortex following occurrence in the endopiriform nucleus. A buildup in population activity preceded the onset of all-or-none epileptiform events in the endopiriform nucleus. Epileptiform events could be triggered by local application of glutamate in the endopiriform nucleus and adjacent claustrum, but not from the piriform cortex. Finally, local application of Co2+ in the endopiriform nucleus, but not in the piriform cortex or elsewhere in the slices, blocked the occurrence of epileptiform events. 4. Additional experiments were performed to further characterize the generation process. 6,7-Dinitroquinoxaline-2,3-dione (DNQX) blocked epileptiform events and the preceding accelerating buildup in multiunit activity at a concentration below that required to block the monosynaptic excitatory postsynaptic potential (EPSP). This suggests that EPSPs mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors underlie epileptiform events in slices of piriform cortex, and that multisynaptic interactions within the endopiriform nucleus are required for generation of these epileptiform EPSPs. By contrast, block of N-methyl-D-aspartate (NMDA) receptors decreased the amplitude of epileptiform EPSPs but did not block their occurrence, indicating that NMDA receptors contribute to generation but are not required. When membrane potential was depolarized to increase driving force, fast inhibitory postsynaptic potentials were found to consistently accompany the buildup process and epileptiform EPSPs. This indicates that if initiation of epileptiform activity in the endopiriform nucleus results from a compromise in feedback inhibition, this compromise is partial rather than complete. 5. Epileptiform EPSPs in slices of piriform cortex from kindled rats displayed similarities in properties, locus of origin, and mechanism of generation to those previously studied in slices from normal rats in which epileptiform activity was induced by a brief period of bursting activity. These similarities suggest that study of bursting-induced epileptiform EPSPs may provide insight into certain aspects of kindling-induced epileptogenesis.

Amygdala↗
PubMed2000

Functional downregulation of GluR2 in piriform cortex of kindled animals.

We have previously shown kindling-induced downregulation of the AMPA receptor GluR2 subunit in piriform cortex, as measured by Western blotting. In the present studies, we performed whole-cell patch clamp analysis of AMPA receptor-mediated currents from kindled and control animals to determine if the downregulation observed previously had any functional significance. These experiments were done in the absence and presence of N-hydroxyphenylpropanoyl spermine (HPPS), a polyamine that blocks currents through AMPA receptors lacking GluR2. We report that AMPA receptor-mediated currents recorded from piriform cortex layer II pyramidal cells in slices from animals kindled to 10 fully generalized seizures were blocked by HPPS. In contrast, application of HPPS had no effect on current amplitude in control animals, or in animals that had not been fully kindled. Western blotting revealed that decreases in GluR2 were seen in animals that had experienced at least one fully generalized seizure, but were not observed at earlier stages of kindling development. The increased polyamine sensitivity of AMPA receptor-mediated currents in kindled animals is consistent with the hypothesis that kindling induces formation of AMPA receptors that lack GluR2 in piriform cortex pyramidal cells. It has been demonstrated that polyamine sensitivity is directly correlated with the calcium permeability of the AMPA receptor, suggesting that kindling results in the formation of AMPA receptors that are calcium-permeable. Increases in intracellular calcium through these receptors could act as a second messenger and play a role in the initiation of long-term changes that contribute to the pathogenesis of kindling-induced epilepsy.

Animals↗
PubMed2001

A new subdivision of anterior piriform cortex and associated deep nucleus with novel features of interest for olfaction and epilepsy.

The anterior part of the piriform cortex (the APC) has been the focus of cortical-level studies of olfactory coding and associative processes and has attracted considerable attention as a result of a unique capacity to initiate generalized tonic-clonic seizures. Based on analysis of cytoarchitecture, connections, and immunocytochemical markers, a new subdivision of the APC and an associated deep nucleus are distinguished in the rat. As a result of its ventrorostral location in the APC, the new subdivision is termed the APC(VR). The deep nucleus is termed the pre-endopiriform nucleus (pEn) based on location and certain parallels to the endopiriform nucleus. The APC(VR) has unique features of interest for normal function: immunostaining suggests that it receives input from tufted cells in the olfactory bulb in addition to mitral cells, and it provides a heavy, rather selective projection from the piriform cortex to the ventrolateral orbital cortex (VLO), a prefrontal area where chemosensory, visual, and spatial information converges. The APC(VR) also has di- and tri-synaptic projections to the VLO via the pEn and the submedial thalamic nucleus. The pEn is of particular interest from a pathological standpoint because it corresponds in location to the physiologically defined "deep piriform cortex" ("area tempestas") from which convulsants initiate temporal lobe seizures, and blockade reduces ischemic damage to the hippocampus. Immunostaining revealed novel features of the pEn and APC(VR) that could alter excitability, including a near-absence of gamma-aminobutyric acid (GABA)ergic "cartridge" endings on axon initial segments, few cholecystokinin (CCK)-positive basket cells, and very low gamma-aminobutyric acid transporter-1 (GAT1)-like immunoreactivity. Normal functions of the APC(VR)-pEn may require a shaping of neuronal activity by inhibitory processes in a fashion that renders this region susceptible to pathological behavior.

Animals↗
PubMed1996

Epileptiform activity in the piriform cortex of the in vitro isolated guinea pig brain preparation.

Brief intracerebral injections of bicuculline in the anterior portion of the piriform cortex of the isolated guinea pig brain preparation induce a transient, localized disinhibition confined to the site of drug application. The epileptiform activity generated at the bicuculline focus propagates and induces secondary excitability changes in remote cortical regions within the olfactory lobe. Long lasting changes in synaptic potentials were observed in the posterior piriform cortex, where long-projective cortico-cortical fibers originating from the site of bicuculline injection terminate. The activation of rhythmic, transient afterdischarges at the bicuculline focus was critical for the development of persistent 'epileptiform' associative synaptic potentials in remote cortical regions. When transient afterdischarges were prevented, epileptiform associative potentials in the posterior piriform cortex appeared only transiently and vanished within 20 min. The persistent secondary changes in synaptic excitability that occur in cortical regions distant from the acutely-induced primary epileptic focus may represent one of the transition mechanisms toward chronic epileptogenesis.

Animals↗
PubMed1987

Role of dorsomedial thalamic nucleus and piriform cortex in processing olfactory information.

Four experiments were conducted to characterize the role of primary and secondary olfactory projection areas (piriform cortex and dorsomedial thalamic nucleus (DMN] in olfactory information processing. Rats had to learn to discriminate between odors that were simultaneously released from different arms of an automated olfactory maze. When standard training conditions were used, damage of the DMN severely impaired both preoperatively trained and naive animals in acquiring an odor discrimination set (i.e. in most problems no learning was demonstrated). An additional group of DMN animals that received 4 times the standard amount of daily trials was unable to acquire the first two problems but successfully solved the third and all subsequent discriminations. Analysis of performance patterns suggested that destruction of the DMN initially leads to a strong procedural impairment that can be overcome by extensive training. After solving the third problem the animals with DMN damage required much less training to reach the learning criterion but generally made more errors than controls. Transfer of savings rarely occurred when a problem was repeated. Whether this secondary learning deficit observed in later discriminations is due to a specific effect of the lesion on the encoding of olfactory cues and thus on memory formation, or due to a disturbance in the regulation of emotional factors such as motivation, arousal, and attention is discussed. Lesions of the thalamus that spared the DMN had no effect on learning or retention of olfactory discriminations. Animals with ablations of the piriform cortex only acquired odor discriminations if they had been trained in the olfactory maze before the lesion. Moreover, their performance depended on the odor quality: they had great difficulty learning complex cues consisting of several odorants and learned simple odors virtually identical to control rats. The results indicate that an intact piriform cortex is needed to acquire the procedures involved to perform an olfactory discrimination task as well as to build neural representations of olfactory cues.

Animals↗
PubMed1980

The organization of projections from the olfactory bulb to the piriform cortex and olfactory tubercle in the rat.

The organization of the projection of olfactory bulb output cells was studied in the rat by injection of horseradish peroxidase (HRP) into the piriform cortex or olfactory tubercle. We made single HRP injections into small cuts in the fiber layer of the projection areas in order to enhance uptake by axons and to confine the region of HRP uptake. Following most of these injections, HRP-labeled axons could be traced in discrete fascicles through the fiber layer of the cortex or tubercle. These observations indicate that axons innervating the piriform cortex do not emit many long collaterals after they leave the lateral olfactory tract. HRP-labeled cells were generally observed throughout the ipsilateral olfactory bulb, but there were regions of greater density of labeled cells that differed in the various brains. The differences among the distributions of labeled mitral and tufted cells were analyzed statistically in 39 brains to test whether they varied systematically with injection site. In these analyses, the olfactory bulb was divided into 30 standard regions, and the labeled cells in each regions were counted. The distributions of labeled cells were similar for brains where injections were made into similar regions of the piriform cortex. The variations in density of labeled cells of the dorsal and anterior regions of the olfactory bulb were most strongly correlated with the positions of cortical injections. In contrast, the posterior medial regions of the bulb were heavily labeled after almost all injections. The ventral portions of the olfactory bulb were most heavily labeled after injections into the olfactory tubercle.

Animals↗
PubMed2000

High susceptibility of the anterior and posterior piriform cortex to induction of convulsions by bicuculline.

Accumulating evidence suggests that the piriform cortex (PC) plays a critical role in the development of limbic motor seizures. In the anterior piriform cortex (aPC), a functionally defined, discrete epileptogenic site has been previously identified by unilateral microinjection of bicuculline in Sprague-Dawley (SD) rats and termed the 'area tempestas' (AT). Compared to this site in the aPC, more posterior PC sites, particularly a site in the transition zone between the posterior and aPC (central PC) exhibited a greater susceptibility to electrical stimulation. However, it is not known whether central and posterior sites in the PC differ from the aPC, including the AT, with regard to their sensitivity to bicuculline. In the present study, unilateral focal microinfusion of picomole quantities of bicuculline induced behavioural (focal and generalized) seizures in deep layers of all parts of the PC in two rat strains, Wistar and SD. The incidence of generalized seizures was higher in the AT of SD rats, but no such difference was seen in Wistar rats, arguing against the previous proposal that the rat AT is unique in its sensitivity to induction of seizures by bicuculline compared to other locations within or outside of the PC. Injection of biotin-dextran in PC seizure-sensitive sites in SD rats showed clear differences in anterograde and retrograde labelling between the different PC sites. Therefore, although it was possible to evoke generalized seizures from all parts of the PC, the anatomical connections of the bicuculline injection sites were qualitatively different. The results suggest that the deep layers of the entire PC are highly sensitive to seizure induction by bicuculline, thus substantiating the notion that the PC may be important in seizure generation and propagation.

Amygdala↗
PubMed1998

Reduced after-hyperpolarization in rat piriform cortex pyramidal neurons is associated with increased learning capability during operant conditioning.

Learning-related cellular modifications were studied in the rat piriform cortex. Water-deprived rats were divided to three groups: 'trained' rats were trained in a four-arm maze to discriminate positive cues in pairs of odours, 'control' rats were 'pseudo-trained' by random water rewarding, and 'naive' rats were water-deprived only. In one experimental paradigm, the trained group was exposed to extensive training with rats learning to discriminate between 35 and 50 pairs of odours. Piriform cortex pyramidal neurons from 'trained', 'control' and 'naive' rats did not differ in their passive membrane properties and single spike characteristics. However, the after-hyperpolarizations (AHPs) that follow six-spike trains were reduced after 'extensive training' by 43% and 36% compared with 'control' and 'naive', respectively. This effect was not observed in the piriform cortex of another group of rats, in which hyperexcitability was induced by chemical kindling. In another experimental paradigm rats were trained only until they demonstrated 'rule learning', usually after discriminating between one and two pairs of odours ('mild training'). In this experiment, a smaller, yet significant, reduction (20%) in AHPs was observed. AHP reduction was apparent in most of the sampled neurons. AHP remained reduced up to 3 days after the last training session. 5 days or more after the last training session, AHP amplitude recovered to pre-training value and did not differ between 'trained' rats and the others. Accordingly, training suspension for 5 days or more resulted in slower learning of novel odours. We suggest that increased neuronal excitability, manifested as reduced AHP, is related to the ability of the cortical network to enter a 'learning mode' which creates favourable conditions for enhanced learning capability.

Animals↗
PubMed1997

Binaral interactions in the rat piriform cortex.

Single-unit recordings were made from layer II/III anterior piriform cortex (aPCX) neurons in adult Wistar rats to examine odor response patterns to unilaterally and bilaterally delivered stimuli. Isoamyl acetate odor stimulation was presented either unilaterally through tubes inserted into the external nares, or bilaterally during unilateral olfactory bulb lidocaine infusions. Olfactory bulb multiunit or slow-wave activity was recorded simultaneously bilaterally to monitor selectivity of unilateral odor stimulation. The results demonstrate that 1) commissural input to aPCX neurons is sufficient to drive odor responses, and 2) aPCX neurons can be classified on the basis of spatial receptive field type. These receptive fields include cells that respond 1) selectively to ipsilateral stimulation, 2) selectively to contralateral stimulation, 3) to either ipsilateral or contralateral stimulation, and 4) selectively to bilateral stimulation. The potential functions of binaral convergence in the piriform cortex are discussed, and may include enhancement of perceived odor intensity and bilateral access to olfactory memory.

Anesthetics, Local↗
PubMed1986

Ultrastructural analysis of synaptic relationships of intracellularly stained pyramidal cell axons in piriform cortex.

Axons of pyramidal cells in piriform cortex stained by intracellular injection of horseradish peroxidase (HRP) have been analyzed by light and electron microscopy. Myelinated primary axons give rise to extensive, very fine caliber (0.2 micron) unmyelinated collaterals with stereotyped radiating branching patterns. Serial section electron microscopic analysis of the stained portions of the collateral systems (initial 1-2 mm) revealed that they give rise to synaptic contacts on dendritic spines and shafts. These synapses typically contain compact clusters of large, predominantly spherical synaptic vesicles subjacent to asymmetrical contacts with heavy postsynaptic densities. On the basis of comparisons with Golgi material and intracellularly stained dendrites, it was concluded that dendritic spines receiving synapses from the proximal portions of pyramidal cell axon collaterals originate primarily from pyramidal cell basal dendrites. Postsynaptic dendritic shafts contacted closely resemble dendrites of probable GABAergic neurons identified in antibody and [3H]-GABA uptake studies. Electron microscopic examination of pyramidal cell axon initial segments revealed a high density of symmetrical synaptic contacts on their surfaces. Synaptic vesicles in the presynaptic boutons were small and flattened. It is concluded that pyramidal cells synaptically interact over short distances with other pyramidal cells via basal dendrites and with deep nonpyramidal cells that probably include GABAergic cells mediating a feedback inhibition. This contrasts with long associational projections of pyramidal cells that terminate predominantly on apical dendrites of other pyramidal cells.

Animals↗
PubMed2000

Comparison of odor receptive field plasticity in the rat olfactory bulb and anterior piriform cortex.

Recent work in the anterior piriform cortex (aPCX) has demonstrated that cortical odor receptive fields are highly dynamic, showing rapid changes of both firing rate and temporal patterning within relatively few inhalations of an odor, despite relatively maintained, patterned input from olfactory bulb mitral/tufted cells. The present experiment examined the precision (odor-specificity) of this receptive field plasticity and compared it with the primary cortical afferent, olfactory bulb mitral/tufted cells. Adult Long-Evans hooded rats, urethan anesthetized and freely breathing, were used for single-unit recording from mitral/tufted and aPCX layer II/III neurons. Partial mapping of receptive fields to alkane odors (pentane, heptane, and nonane) was performed before and immediately after habituation (50-s exposure) to one of the alkanes. The results demonstrated that odor habituation of aPCX responses was odor specific, with minimal cross-habituation between alkanes differing by as few as two carbons. Mitral/tufted cells, however, showed strong cross-habituation within the odor set with the most profound cross effects to carbon chains shorter than the habituating stimulus. The results suggest that although mitral/tufted cells and aPCX neurons have roughly similar odor receptive fields, aPCX neurons have significantly better odor discrimination within their receptive field. The results have important implications for understanding the underlying bases of receptive fields in olfactory system neurons and the mechanisms of odor discrimination and memory.

Action Potentials↗
PubMed2004

Chronic restraint stress and chronic corticosterone treatment modulate differentially the expression of molecules related to structural plasticity in the adult rat piriform cortex.

Stress and stress-related hormones induce structural changes in neurons of the adult CNS. Neurons in the hippocampus, the amygdala and the prefrontal cortex undergo neurite remodeling after chronic stress. In the hippocampus some of these effects can be mimicked with chronic administration of adrenal steroids. These changes in neuronal structure may be mediated by certain molecules related to plastic events such as the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). The expression of PSA-NCAM persists in the adult hippocampus and it is up-regulated after chronic stress. The piriform cortex also displays considerable levels of PSA-NCAM during adulthood and indirect evidence suggests that it may also be the target of stress and stress related-hormones. Using immunohistochemistry we have studied the expression of PSA-NCAM and doublecortin (DCX; another protein implicated in neuronal structural plasticity) in the piriform cortex of adult rats subjected either to 21 days of chronic restraint stress or to oral corticosterone administration during the same period. Our results indicate that chronic stress and chronic corticosterone administration have differential effects on the expression of PSA-NCAM and DCX. While chronic stress increases the number of PSA-NCAM- and DCX-immunoreactive cells in the piriform cortex layer II, chronic corticosterone administration decreases these numbers. These findings indicate that stress and adrenal steroids affect the piriform cortex and suggest that in this region, as in the hippocampus, they may induce structural changes. This is a potential mechanism by which stress and corticosterone modulate functions of this limbic region, such as its participation in olfactory memory.

Animals↗
PubMed1988

The piriform cortex is not a direct olfactory relay to the mediodorsal thalamic nucleus in cats and rabbits.

Following injections of horseradish peroxidase into the mediodorsal thalamic nucleus (MD), retrogradely labeled cells were found in various areas in the cat and rabbit. Among these, olfactory-related areas to which the olfactory bulb projects directly or indirectly via the piriform cortex were the olfactory tubercle, amygdala and insular cortex, while no labeled cells were detected in the piriform cortex and endopiriform nucleus in both species. These results indicate that the piriform cortex and endopiriform nucleus do not send their axons directly to the MD.

Amygdala↗
PubMed2003

NMDA systems in the amygdala and piriform cortex and nicotinic effects on memory function.

Both nicotinic cholinergic and NMDA glutaminergic systems are important for memory function. Nicotine has been found repeatedly to significantly improve working memory performance in the radial-arm maze. The NMDA antagonist dizocilpine has been found to impair working memory performance. There is neuropharmacological evidence that these two systems are functionally related. Nicotine is potent at releasing many transmitters including glutamate. The current study was conducted to examine the interaction of nicotinic and NMDA systems within the amygdala with regard to working and reference memory. Rats were trained on a working/reference procedure on a 16-arm radial maze. After acquisition, local infusion cannulae were implanted bilaterally into the amygdala and piriform cortex using stereotaxic techniques. Then 20 min prior to running the rats on the radial-arm maze, they were injected subcutaneously with (-) nicotine ditartrate at doses of 0 and 0.4 mg/kg. Following this, the rats received local infusions of (+) dizocilpine maleate (MK-801) at doses of 0, 2, 6 and 18 microg per side into the lateral amygdala or piriform cortex 10 min prior to running on the radial-arm maze. Each of the eight nicotine and dizocilpine combinations was administered to each rat in a counterbalanced order. After completion of the drug sessions the rats were sacrificed, and using histological methods the cannulae placements were verified. Acute amygdalar infusions of the NMDA glutamate receptor antagonist dizocilpine induced dose-related working and reference memory deficits in the radial-arm maze. Systemic nicotine was not seen to reverse these effects. Dizocilpine infusions into the adjacent piriform cortex did not impair memory function, supporting the specificity of dizocilpine effects in the amygdala. Latency effects were seen with both drugs in both areas. Latencies were decreased with both systemic nicotine and dizocilpine in both the lateral amygdala and the piriform cortex. This study demonstrated the importance of NMDA glutamate systems in the amygdala for appetitively-motivated spatial memory performance.

Amygdala↗
PubMed1997

Acetylcholine and associative memory in the piriform cortex.

The significance of cholinergic modulation for associative memory performance in the piriform cortex was examined in a study combining cellular neurophysiology in brain slices with realistic biophysical network simulations. Three different physiological effects of acetylcholine were identified at the single-cell level: suppression of neuronal adaptation, suppression of synaptic transmission in the intrinsic fibers layer, and activity-dependent increase in synaptic strength. Biophysical simulations show how these three effects are joined together to enhance learning and recall performance of the cortical network. Furthermore, our data suggest that activity-dependent synaptic decay during learning is a crucial factor in determining learning capability of the cortical network. Accordingly, it is predicted that acetylcholine should also enhance long-term depression in the piriform cortex.

Acetylcholine↗
PubMed2006

Neurogenesis in the adult rat piriform cortex.

Multipotent neural precursors have been suggested to exist in many parts of the adult mammalian brain. In the present study, we characterized the neurogenic potential in the piriform cortex of adult rats. Proliferation rates as detected by 5'-bromodeoxyuridine-labeling proved to be low when compared with the major neurogenic brain regions (i.e. the hippocampus and the subventricular zone). 5'-Bromodeoxyuridine/NeuN-labeling in accordance with doublecortin, polysialylated neural cell adhesion molecule, and TUC-4-labeling indicated that neuronal differentiation of newborn cells occurs predominantly in layer II of the piriform cortex. Many of the cells exhibited a pyramidal cell morphology. The lack of 5'-bromodeoxyuridine/NeuN-labeled cells 12 weeks after 5'-bromodeoxyuridine administration argued against long-term survival of newborn neurons in the piriform cortex.

Animals↗